Topographic analysis of somatosensory evoked potentials in patients with well-localized thalamic infarctions

After stimulation of the median nerve, three major negative peaks (NI, NII and NIII) of somatosensory evoked potentials (SEP) have different latencies along the longitudinal array of scalp electrodes: NI and NII at frontal electrodes have the shortest latency (N17, N29). There is a progressive delay toward the central (N19, N32) and parietal areas (N20, N34). NIII (N60) latency differs from one electrode to another but without consistent anterior-posterior latency shift. A variety of SEP abnormalities was observed in 17 patients with non-hemorrhagic thalamic lesions reflecting a disturbance of the complex intra-thalamic and afferent and efferent thalamic pathways. When the lesions were classified into 5 groups according to the presumed vascular territories involved, there were general but not specific characteristics of SEP abnormalities in each group of patients. In four patients with lesions involving primary sensory nuclei and presenting with the thalamic syndrome or the loss of all modalities of sensation, all SEP components after P14 were absent when the affected arm was stimulated. NI peaks were intact in two patients with thalamic sensory lacunes but NII was delayed. NI was present but delayed in three patients with anterior thalamic lesions not involving primary sensory nuclei. In patients with medial thalamic lesions, delayed central NIII was a common finding. In patients with posterior capsule or lateral thalamus lesions either NII and NIII or NIII alone were affected. NI was also affected in some with sparing of the frontal component (N17). These complex relationships between the types of SEP abnormalities and thalamic lesions are compatible with the presence of multiple, at least partially independent, thalamic generators and thalamocortical projection systems mediating regionally specific SEP components.